The endoscopic picture of compression stenosis is that of an elliptical or scabbard-shaped lumen when the bronchus is at rest or during inspiration. Concentric funnel-like compression stenosis, while rare, may be produced by annular growths.

Treatment of Compression Stenoses of the Trachea.—If the thymus be at fault, rapid amelioration of symptoms follows roentgenray or radium therapy. Tracheotomy and the insertion of the long cane-shaped cannula (Fig. 104) past the compressed area is required in the cases caused by conditions less amenable to treatment than thymic enlargement. Permanent cure depends upon the removability of the compressive mass. Should the bronchi be so compressed by a benign condition as to prevent escape of secretions from the subjacent air passages, bronchial intubation tubes may be inserted, and, if necessary, worn constantly. They should be removed weekly for cleansing and oftener if obstructed.

Influenzal Laryngotracheobronchitis.—Influenzal infection, not always by the same organism, sweeps over the population, attacking the air passages in a violent and quite characteristic way. Bronchoscopy shows the influenzal infection to be characterized by intense reddening and swelling of the mucosa. In some cases the swelling is so great as to necessitate tracheotomy, or intubation of the larynx; and if the edema involve the bronchi, occlusion may be fatal. Hemorrhagic spots and superficial erosions are commonly seen, and a thick, tenacious exudate, difficult of expectoration, lies in patches in the trachea. Infants may asphyxiate from accumulation of this secretion which they are unable to expel. The differential diagnosis from diphtheria is sometimes difficult. The absence of true membrane and the failure to find diphtheria bacilli in smears taken from the trachea are of aid but are not infallible. In doubtful cases, the administration of diphtheria antitoxin is a wise precaution pending the establishment of a definite diagnosis. The pseudomembrane sometimes present in influenzal tracheobronchitis is thinner and less pulpy than that of the earlier stages of diphtheria. The casts of the later stages do not occur in influenzal tracheobronchitis (Bibliography I, p. 480).

Edematous Tracheobronchitis.—This is chiefly observed in children. The most frequently encountered form is the epidemic disease to which the name "Influenza" has been given (q.v. supra). The only noticeable difference between the epidemic and the sporadic cases is in the more general susceptibility to the infective agent, which gives the influenzal form an appearance of being more virulently infective. Possibly the sporadic form is simply the attack of children not immunized by a previous attack during an epidemic.

There is another form of edematous tracheobronchitis often of great severity and grave prognosis, that results from the aspiration of irritating liquids or vapors, or of certain organic substances such as peanut kernels, watermelon seeds, etcetera. Tracheotomy should be done if marked dyspnea be present. Secretions can then be easily removed and medication in the form of oily solutions be instilled at will into the trachea. In the Bronchoscopic Clinic many children have been kept alive for days, and their lives finally saved by aspiration of thick, tough, sometimes clotted and crusted secretions, with the aspirating tube (Fig. 10). It is better in these cases not to pass the bronchoscope repeatedly. If, however, evidences of obstruction remain, after aspiration, it is necessary to see the nature of the obstruction and relieve it by removal, dilatation, or bronchial intubation as the case may require. It is all a matter of "plumbing" i.e., clearing out the "pipes," and maintaining a patulous airway.

Tracheobronchial Diphtheria.—Urgent dyspnea in diphtheria when no membrane and but slight lessening of the laryngeal airway is seen, calls for bronchoscopy. Many lives have been saved by the bronchoscopic removal of membrane obstructing the trachea or bronchi. In the early stages, pulpy masses looking like "mother" of vinegar are very obstructive. Later casts of membrane may simulate foreign bodies. The local application of diphtheria antitoxin to the trachea and bronchi has also been recommended. A preparation free from a chemical irritant should be selected.

Abscess of the Lung.—If of foreign-body origin, pulmonary abscess almost invariably heals after the removal of the object and a regime of fresh air and rest, without local measures of any kind. Acute pulmonary abscess from other causes may require bronchoscopic drainage and gentle dilatation of the swollen and narrowed bronchi leading to it. Some of these bronchi are practically fistulae. Obstructive granulations should be removed with crushing, not biting forceps. The regular foreign-body forceps are best for this purpose. Caution should be used as to removal of the granulations with which the abscess "cavity" is filled in chronic cases. The term "abscess" is usually loosely applied to the condition of drowned lung in which the pus has accumulated in natural passages, and in which there is neither a new wall nor a breaking down of normal walls. Chronic lung-abscess is often successfully treated by weekly bronchoscopic lavage with 20 cc. or more of a warm, normal salt solution, a 1:1000 watery potassium permanganate solution, or a weak iodine solution as in the following formula: Rx. Monochlorphenol (Merck) .12 Lugol's solution 8.00 Normal salt solution 500.

Perhaps the best procedure is to precede medicinal applications by the clearing out of the purulent secretions by aspiration with the aspirating bronchoscope and the independent aspirating tube, the latter being inserted into passages too small to enter with the bronchoscope, and the endobronchial instillation of from 10 to 30 cc. of the medicament. The following have been used: Argyrol, 1 per cent watery solution; Silvol, 1 per cent watery solution; Iodoform, oil emulsion 10 per cent; Guaiacol, 10 per cent solution in paraffine oil; Gomenol, 20 per cent solution in oil; or a bismuth subnitrate suspension in oil. Robert M. Lukens and William F. Moore of the Bronchoscopic Clinic report excellent results in post-tonsillectomy abscesses from one tenth of one per cent phenol in normal salt solution with the addition of 2 per cent Lugol's solution. Chlorinated solutions are irritating, and if used, require copious dilution. Liquid petrolatum with a little oil of eucalyptus has been most often the medium.

Gangrene of the Lung.—Pulmonary gangrene has been followed by recovery after the endobronchial injection of oily solutions of gomenol and guaiacol (Guisez). The injections are readily made through the laryngoscope without the insertion of a bronchoscope. A silk woven catheter may be used with an ordinary glass syringe or a long-nozzled laryngeal syringe, or a bronchoscopic syringe may be used.

Lung-mapping by a roentgenogram taken promptly after the bronchoscopic insufflation of bismuth subnitrate powder or the injection of a suspension of bismuth in liquid petrolatum is advisable in most cases of pulmonary abscess before beginning any kind of treatment.

Bronchial Stenosis.—Stenosis of one or more bronchi results at times from cicatricial contraction following secondary infection of leutic, tuberculous or traumatic lesions. The narrowing resulting from foreign body traumatism rarely requires secondary dilatation after the foreign body has been removed. Tuberculous bronchial stenoses rarely require local treatment, but are easily dilated when necessary. Luetic cicatricial stenosis may require repeated dilatation, or even bronchial intubation. Endobronchial neoplasms may cause a subjacent bronchiectasis, and superjacent stenosis; the latter may require dilatation. Cicatricial stenoses of the bronchi are readily recognizable by the scarred wall and the absence of rings at or near the narrowing.

Bronchiectasis.—In most cases of bronchiectasis there are strong indications for a bronchoscopic diagnosis, to eliminate such conditions as foreign body, cicatricial bronchial stenosis, or endobronchial neoplasm as etiologic factors. In the idiopathic types considerable benefit has resulted from the endobronchial lavage and endobronchial oily injections mentioned under lung abscess. It is probable that if bronchoscopic study were carried out in every case, definite causes for many so-called "idiopathic" cases would be discovered. Lung-mapping as elsewhere herein explained is invaluable in the study of bronchiectasis.

Bronchial asthma affords a large field for bronchoscopic study. As yet, sufficient data to afford any definite conclusions even as to the endoscopic picture of this disease have not been accumulated. Of the cases seen in the Bronchoscopic Clinic some showed no abnormality of the bronchi in the intervals between attacks, others a chronic bronchitis. In cases studied bronchoscopically during an attack, the bronchi were found filled with bubbling secretions and the mucosa was somewhat cyanotic in color. The bronchial lumen was narrowed only as much as it would be, with the same degree of cough, in any patient not subject to asthma. The secretions were removed and the attack quickly subsided; but no influence on the recurrence of attacks was observed. It is essential that the bronchoscopic studies be made, as were these, without anesthesia, local or general, for it is known that the application of cocain or adrenalin to the larynx, or even in the nose, will, with some patients, stop the attack. When done without local anesthesia, allowance must be made for the reaction to the presence of the tube. In those cases in which other means have failed to give relief, the endobronchial application of novocain and adrenalin, orthoform, propaesin or anesthesin emulsion may be tried. Cures have been reported by this treatment. Argentic nitrate applied at weekly intervals has proven very efficient in some cases. Associated infective disease of the bronchial mucosa brings with it the questions of immunity, allergy, anaphylaxis, and vaccine therapy; and the often present defective metabolism has to be considered.

Autodrownage.—Autodrownage is the name given by the author to the drowning of the patient in his own secretions. Tracheobronchial secretions in excess of the amount required to moisten the inspired air, become, in certain cases, a mechanical menace to life, unless removed. The cough reflex, forced expiration, and ciliary action, normally remove the excess. When these mechanisms are impaired, as in profound asthenia, laryngeal paralysis, laryngeal or tracheal stenosis, etc.; and especially when in addition to a mild degree of glottic stenosis or impaired laryngeal mobility, the secretions become excessive, the accumulation may literally drown the patient in his own secretions. This is illustrated frequently in influenza and arachidic bronchitis. Infants cannot expectorate, and their cough reflex is exceedingly ineffective in raising secretion to the pharynx; furthermore they are easily exhausted by bechic efforts; so that age may be cited as one of the most frequent etiologic factors in the condition of autodrownage. Bronchoscopic sponge-pumping (q.v.) and bronchoscopic aspiration are quite efficient and can save any patient not afflicted with conditions that are fatal by other pathologic processes.

Lues of the Tracheobronchial Tree.—Compared to laryngeal involvement, syphilis of the tracheobronchial tree is relatively rare. The lesions may be gummatous, ulcerative, or inflammatory, or there may be compressive granulomatous masses. Hemoptysis may have its origin from a luetic ulceration. Excision of fungations or of a portion of the margin of the ulceration for biopsy is advisable. The Wassermann and therapeutic tests, and the elimination of tuberculosis will be required for confirmation. Luetic stenoses are referred to above.

Tuberculosis of the Tracheobronchial Tree.—The bronchoscopic study of tuberculosis is very interesting, but only a few cases justify bronchoscopy. The subglottic infiltrations from extensions of laryngeal disease are usually of edematous appearance, though they are much more firm than in ordinary inflammatory edema. Ulcerations in this region are rare, except as direct extensions of ulceration above the cord. The trachea is relatively rarely involved in tuberculosis, but we may have in the trachea the pale swelling of the early stage of a perichondritis, or the later ulceration and all the phenomena following the mixed pyogenic infections. These same conditions may exist in the bronchi. In a number of instances, the entire lumen of the bronchus was occluded by cheesy pus and debris of a peribronchial gland which had eroded through. As a rule, the mucosa of tuberculosis is pale, and the pallor is accentuated by the rather bluish streak of vessels, where these are visible. Erosion through of peri-bronchial or peri-tracheal lymph masses may be associated with granulation tissue, usually of pale color, but occasionally reddish; and sometimes oozing of blood is noticed. A most common picture in tuberculosis is a broadening of the carina, which may be so marked as to obliterate the carina and to bulge inward, producing deformed lumina in both bronchi. Sometimes the lumina are crescentic, the concavity of the crescent being internal, that is, toward the median line. Absence of the normal anterior and downward movement of the carina on deep inspiration is almost pathognomonic of a mass at the bifurcation, and such a mass is usually tuberculous, though it may be malignant, and, very rarely, luetic. The only lesion visible in a tuberculous case may be cicatrices from healed processes. In a number of cases there has been a discharge of pus coming from the upper-lobe bronchus.

[Fig. 96.—The author's tampons for pulmonary hemostasis by bronchoscopic tamponade. The folded gauze is 10 cm. long; the braided silk cord 60 cm. long.]

Hemoptysis.—In cases not demonstrably tuberculous, hemoptysis may require bronchoscopic examination to determine the origin. Varices or unsuspected luetic, malignant, or tuberculous lesions may be found to be the cause. It is mechanically easy to pack off one bronchus with the author's packs (Fig. 96) introduced through the bronchoscope, but the advisability of doing so requires further clinical tests.

Angioneurotic Edema.—Angioneurotic edema manifests itself by a pale or red swollen mucosa producing stenosis of the lumen. The temporary character of the lesion and its appearance in other regions confirm the diagnosis.

Scleroma of the trachea is characterized by infiltration of the tracheal mucosa, which greatly narrows the lumen. The infiltration may be limited in area and produce a single stricture, or it may involve the entire trachea and even close a bronchial orifice. Drying and crusting of secretions renders the stenosis still more distressing. This disease is but rarely encountered in America but is not infrequent in some parts of Europe. Treatment consists in the prevention of crusts and their removal. Limited stenotic areas may yield to bronchoscopic bouginage. Urgent dyspnea calls for tracheotomy. Radium and roentgenray therapy have been advised, and cure has been reported by intravenous salvarsan treatment (see article by S. Shelton Watkins, on Scleroma in Surg. Gynecol. and Obst., July, 1921, p. 47).

Atrophic tracheitis, with symptoms quite similar to atrophic rhinitis is a not unusual accompaniment of the nasal condition. It may also exist without nasal involvement. On tracheoscopy the mucosa is thinned, pale and dry, and is covered with patches of thick mucilaginous secretion and crusts. Decomposition of secretion produces tracheal "ozena," while the accumulated crusts give rise to the sensation of a foreign body and may seriously interfere with respiration, making bronchoscopic removal imperative. The associated development of tracheal nodular enchondromata has been described. The internal administration of iodine and the intratracheal injection of bland oily solutions of menthol, guaiacol, or gomenol are helpful.



[235] CHAPTER XXX—DISEASES OF THE ESOPHAGUS

The more frequent causes of the one common symptom of esophageal disease, dysphagia, are included in the list given below. To avoid elaboration and to obtain maximum usefulness as a reminder, overlapping has not been eliminated. 1. Anomalies. 2. Esophagitis, acute. 3. Esophagitis, chronic. 4. Erosion. 5. Ulceration. 6. Trauma. 7. Stricture, congenital. 8. Stricture, spasmodic, including cramp of the diaphragmatic pinchcock. 9. Stricture, inflammatory. 10. Stricture, cicatricial. 11. Dilatation, local. 12. Dilatation, diffuse. 13. Diverticulum. 14. Compression stenosis. 15. Mediastinal tumor. 16. Mediastinal abscess. 17. Mediastinal glandular mass. 18. Aneurysm. 19. Malignant neoplasm. 20. Benign neoplasm. 21. Tuberculosis. 22. Lues. 23. Actinomycosis. 24. Varix. 25. Angioneurotic edema. 26. Hysteria. 27. Functional antiperistalsis. 28. Paralysis. 29. Foreign body in (a) pharynx, (b) larynx, (c) trachea, (d) esophagus.



[236] Diagnosis.—The swallowing function can be studied only with the fluoroscope; esophagoscopy for diagnosis, should therefore always be preceded by a fluoroscopic study of deglutition with a barium or other opaque mixture and examination of the thoracic organs to eliminate external pressure on the esophagus as the cause of stenosis. Complete physical examination and Wassermann reaction are further routine preliminaries to any esophagoscopy. Special laboratory tests are done as may be indicated. The physical examination is meant to include a careful examination of the lips, tongue, palate, pharynx, and a mirror examination of the larynx when age permits.

Indications for Esophagoscopy in Disease.—Any persistent abnormal sensation or disturbance of function of the esophagus calls for esophagoscopy. Vague stomach symptoms may prove to be esophageal in origin, for vomiting is often a complaint when the patient really regurgitates.

Contraindications to Esophagoscopy.—In the presence of aneurysm, advanced organic disease, extensive esophageal varicosities, acute necrotic or corrosive esophagitis, esophagoscopy should not be done except for urgent reasons, such as the lodgment of a foreign body; and in this case the esophagoscopy may be postponed, if necessary, unless the patient is unable to swallow fluids. Esophagoscopy should be deferred, in cases of acute esophagitis from swallowing of caustics, until sloughing has ceased and healing has strengthened the weak places. The extremes of age are not contraindications to esophagoscopy. A number of newborn infants have been esophagoscoped by the author; and he has removed foreign bodies from patients over 80 years of age.

Water starvation makes the patient a very bad surgical subject, and is a distinct contraindication to esophagoscopy. Water must be supplied by means of proctoclysis and hypodermoclysis before any endoscopic or surgical procedure is attempted. If the esophageal stenosis is not readily and quickly remediable, gastrostomy should be done immediately. Rectal feeding will supply water for a limited time, but for nutrient purposes rectal alimentation is dangerously inefficient.

Preliminary examination of the pharynx and larynx with tongue depressor should always precede esophagoscopy, for any purpose, because the symptoms may be due to laryngeal or pharyngeal disease that might be overlooked in passing the esophagoscope. A high degree of esophageal stenosis results in retention in the suprajacent esophagus of the fluids which normally are continually flowing downward. The pyriform sinuses in these cases are seen with the laryngeal mirror to be filled with frothy secretion (Jackson's sign of esophageal stenosis) and this secretion may sometimes be seen trickling into the larynx. This overflow into the larynx and lower air passages is often the cause of pulmonary symptoms, which are thus strictly secondary to the esophageal disease.

ANOMALIES OF THE ESOPHAGUS

Congenital esophagotracheal fistulae are the most frequent of the embryonic developmental errors of this organ. Septic pneumonia from the entrance of fluids into the lungs usually causes death within a few weeks.

Imperforate esophagus usually shows an upper esophageal segment ending in a blind pouch. A lower segment is usually present and may be connected with the upper segment by a fistula.

Congenital stricture of the esophagus may be single or multiple, and may be thin and weblike, or it may extend over a third or more of the length of the esophagus. It may not become manifest until solids are added to the child's diet; often not for many months. The lodgment of an unusually large bolus of unmasticated food may set up an esophagitis the swelling of which may completely close the lumen of the congenitally narrow esophagus. It is not uncommon to meet with cases of adults who have "never swallowed as well as other people," and in whom cicatricial and spasmodic stenosis can be excluded by esophagoscopy, which demonstrates an obvious narrowing of the esophageal lumen. These cases are doubtless congenital.

Webs in the upper third of the esophagus are best determined by the passage of a large esophagoscope which puts the esophagus on the stretch. The webs may be broken by the insertion of a closed alligator forceps, which is then withdrawn with opened blades. Better still is the dilator shown in Fig. 26. This retrograde dilatation is relatively safe. A silk-woven esophagoscopic bougie or the metallic tracheal bougie may be used, with proper caution. Subsequent dilatation for a few times will be required to prevent a reproduction of the stenosis.

Treatment of Esophageal Anomalies.—Gastrostomy is required in the imperforate cases. Esophagoscopic bouginage is very successful in the cure of all cases of congenital stenosis. Any sort of lumen can be enlarged so any well masticated food can be swallowed. Careful esophagoscopic work with the bougies (Fig. 40) will ultimately cure with little or no risk of mortality. Any form of rapid dilatation is dangerous. Congenital stenosis, if not an absolute atresia, yields more readily to esophagoscopic bouginage than cicatricial stenosis.

RUPTURE AND TRAUMA OF THE ESOPHAGUS

These may be spontaneous or may ensue from the passage of an instrument, or foreign body, or of both combined, as exemplified in the blind attempts to remove a foreign body or to push it downwards. Digestion of the esophagus and perforation may result from the stagnation of regurgitated gastric juice therein. This condition sometimes occurs in profound toxic and debilitated states. Rupture of the thoracic esophagus produces profound shock, fever, mediastinal emphysema, and rapid sinking. Pneumothorax and empyema follow perforation into the pleural cavity. Rupture of the cervical esophagus is usually followed by cervical emphysema and cervical abscess, both of which often burrow into the mediastinum along the fascial layers of the neck. Lesser degrees of trauma produce esophagitis usually accompanied by fever and painful and difficult swallowing.

The treatment of traumatic esophagitis consists in rest in bed, sterile liquid food, and the administration of bismuth subnitrate (about one gramme in an adult), dry on the tongue every 4 hours. Rupture of the esophagus requires immediate gastrostomy to put the esophagus at rest and supply necessary alimentation. Thoracotomy for drainage is required when the pleural cavity has been involved, not only for pleural secretions, but for the constant and copious esophageal leakage. It is not ordinarily realized how much normal salivary drainage passes down the esophagus. The customary treatment of shock is to be applied. No attempt should be made to remove a foreign body until the traumatic lesions have healed. This may require a number of weeks. Decision as to when to remove the intruder is determined by esophagoscopic inspection.

Subcutaneous emphysema does not require puncture unless gaseous, or unless pus forms. In the latter event free external drainage becomes imperative.

ACUTE ESOPHAGITIS

This is usually of traumatic or cauterant origin. If severe or extensive, all the symptoms described under "Rupture of the Esophagus" may be present. The endoscopic appearances are unmistakable to anyone familiar with the appearance of mucosal inflammations. The pale, bluish pink color of the normal mucosa is replaced by a deep-red velvety swollen appearance in which individual vessels are invisible. After exudation of serum into the tissues, the color may be paler and in some instances a typical edema may be seen. This may diminish the lumen temporarily. Folds of swollen mucosa crowd into the lumen if the inflammation is intense. These folds are sometimes demonstrable in the roentgenogram by the bismuth or barium in the creases between which the prominence of the folds show as islands as beautifully demonstrated by David R. Bowen in one of the author's cases. If the inflammation is due to corrosives, a grayish exudate may be visible early, sloughs later.

ULCERATION OF THE ESOPHAGUS

Superficial erosions of the esophagus are by no means an uncommon accompaniment of the stagnation of food and secretions. From the irritation they produce, spastic stenosis may occur, thus constituting a vicious circle; the spasm of the esophagus increases the stagnation which in turn results in further inflammation and ultimate ulceration. Healing of such ulcers may result in cicatricial contraction and organic stenosis. Ulceration may follow trauma by instrument, foreign body, or corrosive.

DIFFERENTIAL DIAGNOSIS OF ULCER OF THE ESOPHAGUS

Simple ulcer requires the exclusion of lues, tuberculosis, epithelioma, endothelioma, sarcoma, and actinomycosis. Simple ulcer of the esophagus is usually associated with stenosis, spastic or organic.

Luetic ulcers commonly show a surrounding inflammatory areola, and they usually have thickened elevated edges, generally free from granulation tissue, with a pasty center not bleeding readily when sponged. The Wassermann reaction may contribute to the diagnosis; but if negative, a thorough and prolonged test with mercury is imperative. It must be remembered that a person with lues may have a simple, mixed, or malignant ulceration of the esophagus, or the three lesions may even be combined. It may be in some cases possible to demonstrate the treponema pallidum in scrapings taken from the ulcer.

The single tuberculous ulcer is usually pale, superficial, and granular in base. If it is a continuation from more extensive extra-esophageal tuberculous ulceration, pale cauliflower granulations may be present. Slight cicatrices may be seen. Tuberculosis in other organs can almost always be demonstrated by roentgenographic, physical, or laboratory studies. Tuberculin tests and animal injection with an emulsion of a specimen of tissue may be required. The specimen must be taken very superficially to avoid risk of perforation.

Sarcomatous ulcers do not differ materially in appearance from those of carcinoma, but they are much more rare.

Carcinomatous ulcer is usually characterized by the very vascular bright red zone, raised edges, fungations, granulation tissue that bleeds freely on the lightest touch, and above all, it is almost invariably situated on an infiltrated base which communicates a feeling of hardness to the pressure of sponges or the esophagoscope itself. A scar may be from the healing of an ulcer from stasis, or one of specific or precancerous character. It may be a cancerous process developing on the site of a scar, so that the presence of scar tissue does not absolutely negative malignancy. As a rule, however, scars are absent in cancer of the esophagus. The firm and sometimes prominent ridge of the crossing of the left bronchus must not be mistaken for infiltration, and the esophagoscopist must be familiar with the normal rigidity of the cricopharyngeus.

[242] Mixed infection gives to all esophageal ulceration a certain uniformity of appearance, so that laboratory studies of smears or histologic and bacteriologic study of tissue specimens taken from fungations or thickened edges are often required to confirm the endoscopic diagnosis. If the edges are thin and flat, the taking of a specimen involves some risk; fungations can be removed without risk; so can nodules, but care must be taken that projecting folds are not mistaken for nodules. It is always wise to push the therapeutic test with potassium iodid and especially mercury in any case of esophageal ulceration unassociated with stasis.

Treatment of Acute and Subacute Inflammation and Ulceration of the Esophagus.—Bismuth subnitrate in doses of about one gramme, given dry on the tongue and swallowed without water, has a local antiseptic and protective action. Its antiseptic power may be enhanced by the addition of calomel to the powder, in such amount as may be tolerated by the bowels. If pain be present the combination of a grain or two of anesthesin or orthoform with the bismuth will be grateful. The local application of argyrol in 25 per cent watery solution is also of great value. The mouth and teeth are to be kept clean with a mouth wash of Dakin's solution, 1 part, to peppermint water, 6 parts. The esophagus must be placed at rest as far as possible by liquid diet or, if need be, by gastrostomy.

CHRONIC ESOPHAGITIS

This is usually a result of stagnation of food or secretion, and will be considered under spasmodic stenosis and diffuse dilatation of the esophagus.

A very marked case with local distress and pain extending through to the back was seen by the author in consultation with Dr. John B. Wright who had made the diagnosis. The patient was a sufferer from ankylostomiasis.

[243] COMPRESSION STENOSIS OF THE ESOPHAGUS

The esophagus may be narrowed by the pressure of any periesophageal disease or anomaly. The lesions most frequently found are: 1. Goiter, cervical or thoracic. 2. Malignancy of any of the intrathoracic viscera. 3. Aneurysm. 4. Cardiac and aortic enlargement. 5. Lymphadenopathies. Hodgkins' disease. Leukemia. Lues. Tuberculosis. Simple infective adenitis. 6. Lordosis. 7. Enlargement of the left hepatic lobe.

Endoscopically, compression stenosis of the esophagus is manifested by a slit-like crevice which occupies the place of the lumen and which does not open up readily before the advancing tube. The long axis of the slit is almost always at right angles to the compressive mass, if the esophageal wall be uninvolved. The covering mucosa may be normal or it may show signs of chronic inflammation. Malignant compressions are characterized by their hardness when palpated with the tube. Associated pressure on the recurrent laryngeal nerve often makes laryngeal paralysis coexistent. The nature of the compressive mass will require for its determination the aid of the roentgenologist, internist, and clinical laboratory. Compression by the enlarged left auricle has been observed a number of times. The presence of aneurysm is a distinct contraindication to esophagoscopy for diagnosis except in case of suspected foreign body.

Treatment of compressive stenosis of the esophagus depends upon the nature of the compressive lesion and is without the realm of endoscopy. In uncertain cases potassium iodid, and especially mercury, should always be given a thorough and prolonged trial; an occasional cure will result. Esophageal intubation is indicated in all conditions except aneurysm. Gastrostomy should be done early when necessary.

DIFFUSE DILATATION OF THE ESOPHAGUS

This is practically always due to stagnation ectasia, which is invariably associated with either organic or "spasmodic" stricture, existing at the time of observation or at some time prior thereto. The dilating effect of the repeatedly accumulated food results in a permanent enlargement, so that the esophagus acts as the reservoir of a large funnel with a very small opening. When food is swallowed the esophagus fills, and the contents trickle slowly through the opening. Gases due to fermentation increase the distension and cause substernal pressure, discomfort, and belching. A very large dilatation of the thoracic esophagus indicates spastic stenosis. Cicatricial stenoses do not result in such large dilatations and the dilatation above a malignant stenosis is usually slight, probably because of its relatively shorter duration.

The treatment of diffuse esophageal dilatation consists in dilating the "diaphragmatic pinchcock" that is, the hiatal esophagus. Chronic esophagitis is to be controlled by esophageal lavage, the regulation of the diet to liquefiable foods and the administration of bismuth subnitrate. The patient can be taught to do the lavage. The local esophagoscopic application of a small quantity of a 25 per cent watery solution of argyrol may be required for the static esophagitis. The redundancy probably never disappears; but functional and subjective cures are usually obtainable.



[245] CHAPTER XXXI—DISEASES OF THE ESOPHAGUS (Continued)

SPASMODIC STENOSIS OF THE ESOPHAGUS

Etiology.—The functional activity of the esophagus is dependent upon reflex action. The food is propulsed in a peristaltic wave by the same mechanism as, and through an innervation (Auerbach and Meissner plexus) similar to that which controls intestinal movements. The vagus also is directly concerned with the deglutitory act, for swallowing is impossible if both vagi are cut. Anything which unduly disturbs this reflex arc may serve as an exciting cause of spasmodic stenosis. Bolting of food, superficial erosions, local esophageal disease, or a small foreign body, may produce spasmodic stenosis. Spasm secondary to disease of the stomach, liver, gall bladder, appendix, or other abdominal organ is clinically well recognized. A perpetuating cause in established cases is undoubtedly "nerve cell habit," and in many cases there is an underlying neurotic factor. Shock as an exciting cause has been well exemplified by the number of cases of phrenospasm developing in soldiers during the World War.

Cricopharyngeal spasmodic stenosis usually presents the subjective symptom of difficulty in starting the bolus of food downward. Once started, the food passes into the stomach unimpeded. Regurgitation, if it occurs, is immediate. The condition consists in a tonic contraction, ahead of the bolus, of the circular fibers of the inferior constrictor known as the cricopharyngeus muscle, or in a failure of this muscle to relax so as to allow the bolus to pass. In either case the disorder may be secondary to an organic lesion. Local malignant disease or foreign bodies may be the cause. Globus hystericus, "lump in the throat," and the sense of constriction and choking during emotion are due to the same spasmodic condition.

Diagnosis.—At esophagoscopy there will be found marked exaggeration of the usual spasm which occurs at the cricopharyngeus during the introduction of the tube. The lumen may assume various shapes, or be so tightly closed that the folds form a mammilliform projection in the center. If the spasm gradually yields, and a full-sized esophagoscope passes without further resistance, it may be stated that the esophagus is of normal calibre, and a diagnosis of spasmodic stenosis can be made. Considerable experience is required to distinguish between normal and pathologic spasm in an unanesthetized individual. To the less experienced esophagoscopist, examination under ether anesthesia is recommended. Deep anesthesia will relax the normal cricopharyngeal reflex closure as well as any abnormal spasm, thus assisting in the differentiation between an organic stricture and one of functional character. Under deep general anesthesia, however, it is impossible to differentiate between the normal reflex and a spasmodic condition, since both are abolished. Many cases of intermittent esophageal stenosis supposed to be spasmodic are due to organic narrowness of lumen plus lodgement of food, obstructive in itself and in the esophagitis resulting from its presence. The organic narrowing, congenital or pathologic, is readily recognizable esophagoscopically.

Treatment.—The fundamental cause of the disturbance of the reflex should be searched for, and treated according to its nature. Purely functional cases are often cured by the passage of a large esophagoscope. Recurrences may require similar treatment.

[247] FUNCTIONAL HIATAL STENOSIS. HIATAL ESOPHAGISMUS. PHRENOSPASM, DIAPHRAGMATIC PINCHCOCK STENOSIS. (SO-CALLED CARDIOSPASM)

There is no sphincteric muscular arrangement at the cardiac orifice of the esophagus, so that spasmodic stenosis at this level is not possible and the term cardiospasm is, therefore, a misnomer. It was first demonstrated by the author that in so-called cardiospasm the functional closure of the esophagus occurred at the diaphragmatic level, and that it was due to the "diaphragmatic pinchcock." Anatomical studies have corroborated this finding by demonstrating a definite sphincteric mechanism consisting of muscle bands springing from the crura of the diaphragm and surrounding the esophagus at the under surface of the hiatus. An inspection of the cadaveric diaphragm from below will demonstrate an arrangement like double shears admirably adapted to this "pinchcock" action. Further confirmation is the fact that all dilatation of the esophagus incident to spasm at its lower extremity is situated above the diaphragm. In passing it may be stated that the pinchcock action, plus the kinking of the esophagus normally prevents regurgitation when a man with a full stomach "stands on his head" or inverts his body. For the upward escape of food from the stomach an involuntary co-ordinated antiperistaltic cycle is necessary. The dilatation resulting from phrenospasm may reach great size (Fig. 96a), and the capacity of the sac may be as much as two liters. While the esophagus is usually dilated, the stomach on the other hand is often contracted, largely from lack of distention by food, but possibly also because of a spastic state due to the same causes as the phrenospasm. Recently Mosher has demonstrated that hepatic abnormality may furnish an organic cause in many cases formerly considered spasmodic.

The symptoms of hiatal esophagismus are variable in degree. Substernal distress, with a feeling of fullness and pressure followed by eructations of gas and regurgitation of food within a period of a quarter of an hour to several hours after eating, are present. If the esophageal dilatation be great, regurgitation may occur only after an accumulation of several days, when large quantities of stale food will be expelled. The general nutrition is impaired, and there is usually the history of weight loss to a certain level at which it is maintained with but slight variation. This is explained by the trickling of liquified food from the esophageal reservoir into the stomach as the spasm intermittently relaxes, this occurring usually before a serious state of inanition supervenes. At times the hiatal spasms are extremely violent and painful, the pain being referred from the xiphoid region to the back, or upward into the neck. Patients are often conscious of the times of patulency of the esophagus; they will know the esophagus to be open and will eat without hesitation, or will refuse food with the certain knowledge that it will not pass into the stomach. Periods of remission of symptoms for months and years are noted. The neurotic character of the lesion in some cases is evidenced by the occasionally sudden and startling cures following a single dilatation, as well as by the tendency to relapse when the individual is subject to what is for him undue nervous tension. In a very few cases, with patients of rather a stolid type, all neurotic tendencies seem to be absent.

The diagnosis of hiatal esophagismus requires the exclusion of local organic esophageal lesions. In the typical case with marked dilatation, the esophagoscopic findings are diagnostic. A white, pasty, macerated mucosa, and normally contracted hiatus esophageus which when found permits the large esophagoscope to pass into the stomach, will be recognized as characteristic by anyone who has seen the condition. In the cases with but little esophageal distension the diagnosis is confirmed by the constancy of the obstruction to a barium mixture at the phrenic level, while at esophagoscopy the usual resistance at the hiatus esophageus is found not to be increased, and no other local lesion is found as the esophagoscope enters the stomach. It is the failure of the diaphragmatic pinchcock to open, as in the normal deglutitory cycle, rather than a spasmodic tightness, that obstructs the food. The presence of organic stenosis at the hiatus may remove the case altogether from the spasmodic class, or a cicatricial or infiltrated narrowing may be the result of static esophagitis. A compressive stenosis due to hepatic abnormality may simulate spasmodic stenosis as shown by Mosher, who believes that 75 per cent of so-called cardiospasms are organic.

Treatment of hiatal esophagismus (so-called cardiospasm) consists in the over-dilatation of the "diaphragmatic pinchcock" or hiatus esophageus, and in proper remedial measures for the removal of the underlying neurosis. The simple passage of the esophagoscope suffices to cure some cases. Further dilatation by endoscopic guidance may be obtained by the introduction of Mosher's divulsor through the esophagoscope, by which accurate placement is obtained. The distension should not usually exceed 25 mm. Numerous water and air bags have been devised for stretching the hiatus, and excellent results have been obtained by their use. Possibly some of the cures have been due to the dilatation of organic lesions, or to the crowding back of an enlarged malposed, or otherwise abnormal left lobe of the liver, which Mosher has shown to be an etiologic factor.

Certain cases prove very obstinate of cure, and require esophageal lavage for the esophagitis, and feedings through the stomach tube to increase nutrition and to dilate the contracted stomach. Gastrostomy for feeding rarely becomes necessary, for a stomach tube can always be placed with the esophagoscope if it will not pass otherwise. Retrograde dilatation with the fingers through a gastrostomy opening has been done, but seems hardly warranted in view of the excellent results obtainable from above. Instructions should be given concerning the proper mastication of food, and during treatment the frequent partaking of small quantities of liquid foods is recommended. Liquids and foods should be neither hot nor cold. The neurologist should be consulted in cases deemed neurotic.

[96a.-Functional hiatal stenosis. Cramp of the diaphragmatic pinchcock (so-called cardiospasm).]

Endocrine imbalance should be investigated and treated, as urged by MacNab.

Esophageal antiperistalsis is the name given by the author to a heretofore undescribed disease associated with regurgitation of food from the esophagus, the food not having reached the stomach. It may be continuous or paroxysmal and may be of so serious a degree as to threaten starvation. The best treatment in severe cases is gastrostomy to put the esophagus at rest. Milder cases get well under liquid diet, rest in bed, endocrine therapy, cure of associated abdominal disease, etcetera.



[251] CHAPTER XXXII—DISEASES OF THE ESOPHAGUS (Continued)

CICATRICIAL STENOSIS OF THE ESOPHAGUS

Etiology.—The accidental swallowing of caustic alkali in solutions of lye or proprietary washing and cleansing powders, is the most frequent cause of cicatricial stenosis. Commercial lye preparations are about 95 per cent sodium hydroxide. The cleansing and washing powders contain from eight to fifty per cent of caustic alkali, usually soda ash, and are sold by grocers everywhere. The labels on their containers not only give no warning of the dangerous nature of the contents nor antidotal advice, but have such directly misleading statements as : "Will not injure the most delicate fabric," "Will not injure the hands," etc. Utensils used to measure or dissolve the powders are afterward used for drinking, without rinsing, and thus the residue of the powder remaining is swallowed in strong solution. At other times solutions of lye are drunk in mistake for water, coffee, or wine. These entirely preventable accidents would be rare if they were as conspicuously labelled "Poison" as is required by law in the case of these and any other poisons, when sold by druggists. The necessity for such labelling is even greater with the lye preparations because they go into the kitchen, whereas the drugs go to the medicine shelf, out of the reach of children. "Household ammonia," "salts of tartar" (potassium carbonate), "washing soda" (sodium carbonate), mercuric chloride, and strong acids are also, though less frequently, the cause of cicatricial esophageal stricture. Tuberculosis, lues, scarlet fever, diphtheria, enteric fever and pyogenic conditions may produce ulceration followed by cicatrices of the esophagus. Spasmodic stenosis with its consequent esophagitis and erosions, and, later, secondary pyogenic infection, may result in serious cicatrices. Peptic ulcer of the lower esophagus may be a cause. The prolonged sojourn of a foreign body is likely to result in cicatricial narrowing.

[FIG. 97.—Schematic illustration of a series of eccentric strictures with interstrictural sacculations, in the esophagus of a boy aged four years. The strictures were divulsed seriatim from above downward with the divulsor, the esophageal wall, D, being moved sidewise to the position of the dotted line by means of a small esophagoscope inserted through the upper stricture, A, after divulsion of the latter.]

Location of Cicatricial Esophageal Strictures.—The strictures are often multiple and their lumina are rarely either central or concentric (Fig. 97). In order of frequency the sites of cicatricial stenosis are: 1. At the crossing of the left bronchus; 2. In the region of the cricopharyngeus; 3. At the hiatal level. Stricture at the cardia has rarely been encountered in the Bronchoscopic Clinic. Stenosis of the pylorus has been noted, but is rare.

Prognosis.—Spontaneous recovery from cicatricial stenosis probably never occurs, and the mortality of untreated small lumen strictures is very high. Blind methods of dilatation are almost certain to result in death from perforation of the esophageal wall, because some pressure is necessary to dilate a stricture, and the point of the bougie, not being under guidance of the eye, is certain at sometime or other to be engaged in a pocket instead of in the stricture. Pressure then results in perforation of the bottom of the pocket (Fig. 98). This accident is contributed to by dilatation with the wrinkled, scarred floor which usually develops above the stricture. Rapid divulsion and internal esophagotomy are mechanically very easily and accurately done through the esophagoscope, and would yield a few prompt cures; but the mortality would be very high. Under certain circumstances, to be explained below, gentle divulsion of the proximal one of a series of strictures has to be done. With proper precautions and a gentle hand, the risk is slight. Under esophagoscopic bouginage the prognosis is favorable as to ultimate cure, the duration of the treatment varying with the number of strictures, the tightness, and the extent of the fibrous tissue-changes in the esophageal wall. Mortality from the endoscopic procedure is almost nil, and if gastrostomy is done early in the tightly stenosed cases, ultimate cure may be confidently expected with careful though prolonged treatment.

[FIG. 98.—Schema illustrating the mechanism of perforation by blind bouginage. On encountering resilient resistance the operator, having a false conception, pushes on the bougie. Perforation results because in reality the bougie is in a pocket of the suprastrictural eccentric dilatation.]

Symptoms.—Dysphagia, regurgitation, distress after eating, and loss of weight, vary with the degree of the stenosis. The intermittency of the symptoms is sometimes confusing, for the lodgment of relatively large particles of food often simulates a spasmodic stenosis, and in fact there is often an element of spasm which holds the foreign body in the strictured area until it relaxes. Static esophagitis results in a swelling of the esophageal walls and a narrowing of the lumen, so that swallowing is more or less troublesome until the esophagitis subsides.

Esophagoscopic Appearances of Cicatricial Stenosis.—The color of the cicatricial area is usually paler than the normal mucosa. The scars may be very white and elevated, or they may be flush with the normal mucosa, or even depressed. Occasionally the cicatrix is annular, but more often it is eccentric and involves only a part of the circumference of the wall. If the amount of scar tissue is small, the lumen maintains its mobility; opens and closes during respiration, cough, and vomiturition. Between two strictures there is often a pouch containing food remnants. It is rarely possible to see the lumen of the second stricture, because it is usually eccentric to the first. Stagnation of food results in superjacent dilatation and esophagitis. Erosions and ulcerations which follow the stagnation esophagitis increase the cicatricial stenosis in their healing.

Differential Diagnosis.—When the underlying condition is masked by inflammation and ulceration, these lesions must be removed by frequent lavage, the administration of bismuth subnitrate with the occasional addition of calomel powder, and the limitation of the diet to strained liquids. The cicatricial nature of the stenosis can then be studied to better advantage. In most cases the cicatrices are unmistakably conspicuous. Spasmodic stenoses are differentiated by the absence of cicatrices and the yielding of the stenosis to gentle but continuous pressure of the esophagoscope. While it is possible that spasmodic stenosis may supplement cicatricial stenosis, it is certainly exceedingly rare. Nearly all of the occasions in which a temporary increase of the stenosis in a cicatricial case is attributed to an element of spasm, the real cause of the intermittency is not spasm but obstruction caused by food. This occurs in three ways: 1. Actual "corking" of the strictured lumen by a fragment of food, in which case intermittency may be due to partial regurgitation of the "corking" mass with subsequent sinking tightly into the stricture. 2. The "cork" may dissolve and pass on through to be later replaced by another. 3. Reactionary swelling of the esophageal mucosa due to stagnation. Here again the obstruction may be prolonged, or it may be quite intermittent, due to a valve-like action of the swollen mucosal surfaces or folds intermittently coming in contact. Cancerous stenosis is accompanied by infiltration of the periesophageal tissue, and usually by projecting bleeding fungations. Cancer may, however, develop on a cicatrix, favored no doubt by chronic inflammation in tissue of low resistance. Compression stenosis of the esophagus is characterized by the sudden transition of the lumen to a linear or crescentic outline, while the covering mucosa is normal unless esophagitis be present. The compressive mass can be detected by the sensation transmitted to the touch by the esophagoscope.

Treatment.—Blind bouginage should be discarded as an obsolete and very dangerous procedure. If the stenosis be so great as to interfere with the ingestion of the required amount of liquids, gastrostomy should be done at once and esophagoscopic treatment postponed until water hunger has been relieved. Gastrostomy aids in the treatment by putting the esophagus at rest, and by affording the means of maintaining a high degree of nutrition unhampered by the variability or efficiency of the swallowing function. Careful diet and gentle treatment will, however, usually avoid gastrostomy. The diet in the gastrostomy-fed patients should be as varied as in oral alimentation; even solids of the consistency of mashed potatoes, if previously forced through a wire gauze strainer, may be forced through the tube with a glass injector. Liquids and readily liquefiable foods are to be given the non-gastrostomized patient, solids being added when demonstrated that no stagnation above the stricture occurs. Thorough mastication and the slow partaking of small quantities at a time are imperative. Should food accumulation occur, the esophagus should be emptied by regurgitation, following which a glassful of warm sodium bicarbonate solution is to be taken, and this also regurgitated if it does not go through promptly. The esophagus is thus lavaged and emptied. In all these cases, whether being fed through the mouth or the gastrostomic tube, it is very important to remember that milk and eggs are not a complete dietary. A pediatrist should be consulted. Prof. Graham has saved the lives of many children by solving the nutritive problems in the cases at the Bronchoscopic Clinic. Fruit and vegetable juices are necessary. Vegetable soups and mashed fruits should be strained through a wire gauze coffee strainer. If the saliva is spat out by the child because it will not go through the stricture the child should be taught to spit the saliva into the funnel of the abdominal tube. This method of improving nutrition was discovered by Miss Groves at the Bronchoscopic Clinic.

Esophagoscopic bouginage with the author's silk-woven steel-shank endoscopic bougies (Fig. 40) has proven the safest and most successful method of treatment. The strictured lumen is to be centered in the esophagoscopic field, and three successively increasing sizes of bougies are used under direct vision. Larger and larger bougies are used at the successive treatments which are given at intervals of from four to seven days. No anesthesia, general or local, is used for esophagoscopic bouginage. The tightness of the grasping of the bougie by the stricture on withdrawal, determines the limitation of sizes to be used. When the upper stricture is dilated, lower ones in the series are taken seriatim. If concentric, two or more closely situated strictures may be simultaneously dilated. For the use of bougies of the larger sizes, the special esophagoscopes with both the light-carrier canal and the drainage canal outside the lumen of the tube are needed. Functional cure is obtained with a relatively small lumen at the point of stenosis. A lumen of 7 mm. will allow the passage of any well masticated food. It is unwise and unsafe to attempt to restore the lumen to its normal anatomic size. In cicatricial stricture cases it is advisable to examine the esophagus at monthly periods for a time after a functional cure has been obtained, in order that tendency to recurrence may be early detected.

Divulsion of an upper stricture may be deemed advisable in order to reach others lower down, especially in cases of multiple eccentric strictures (Fig. 97). This procedure is best done with the author's esophagoscopic divulser, accurately placed by means of the esophagoscope; but divulsion requires the utmost care, and a gentle hand. Even then it is not so safe as esophagoscopic bouginage.

Internal esophagotomy by the string-cutting instruments and esophagotome are relatively dangerous methods, and perhaps yield in the end no quicker results than the slower and safe bouginage per tubam.

Electrolysis has been used with varying results in the treatment of cicatricial stenosis.

Thermic bouginage with electrically heated bougies has been found useful in some cases by Dean and Imperatori.

[258] String-swallowing, with the passage of olives threaded over the string has yielded good results in the hands of some operators. The string may be used to pull up dilators in increasing sizes, introduced through a gastrostomic fistula. The string stretched across the stomach from the cardia to the pylorus, is fished out with the author's pillar retractor, or is found with the retrograde esophagoscope (Fig. 43). The string is attached to a dilator (Fig. 35), and a fresh string is pulled in to replace the one pulled out. This is the safest of the blind methods. It is rarely possible to get a child under two years of age to swallow and tolerate a string. It is better after each treatment to draw the upper end of the string through the nose, as it is not so likely to be chewed off and is less annoying. With the esophagoscope, the string is not necessary, because the lumen of the stricture can be exposed to view by the esophagoscope.

Retrograde esophagoscopy through a gastrostomy wound offers some advantages over peroral treatment; but unless the gastrostomy is high, the procedure is undoubtedly more difficult. The approach to the lowest stricture from below is usually funnel shaped and free from dilatation and redundancy. It must be remembered the stricture seen from below may not be the same one seen from above. Roentgenray examination with barium mixture or esophagoscopes simultaneously in situ above and below are useful in the study of such cases.

Impermeable strictures of the cervical esophagus are amenable to external esophagotomy, with plastic reformation of the esophagus. Those in the middle third have not been successfully treated by surgical methods, though various ingenious operations for the formation of an extrathoracic esophagus have been suggested as means of securing relief. Impermeable strictures of the lower third can with reasonable safety be treated by the Brenneman method, which consists in passing the esophagoscope down to the stricture while the surgeon, inserting his finger up into the esophagus from the stomach, can feel the end of the esophagoscope. An incision through the tissue barrier is then made from below, passing the knife along the finger as a guide. A soft rubber stomach-tube is pulled up from below and left in situ, being replaced at intervals by a fresh one, pulled up from the stomach, until epithelialization of the new lumen is complete. Catheters are used in children. In replacing the catheter or stomach tube the fresh one is attached to the old one by stitching in a loop of braided silk. Frequent esophagoscopic bouginage will be required to maintain the more or less fistulous lumen until it is epithelialized, and in occasional cases, for a long time thereafter.

In cases of absolute atresia the saliva does not reach the stomach. No one realizes the quantity of normal salivary drainage, nor its importance in nutritive processes. Oral insalivation is of little consequence compared to esophagogastric drainage. Gastrostomized children with absolute atresia of the esophagus do not thrive unless they regurgitate the salivary accumulations into the funnel of the gastrostomic feeding tube. This has been abundantly proven by observations at the Bronchoscopic Clinic. My attention was first called to this clinical fact by Miss Frances Groves who has charge of these cases.

Intubation of the esophagus with soft rubber tubes has occasionally proven useful.



[260] CHAPTER XXXIII—DISEASES OF THE ESOPHAGUS (Continued)

DIVERTICULUM OF THE ESOPHAGUS

Diverticula may, and usually do, consist in a pouching by herniation, of the whole thickness of the esophageal wall; or they may be herniations of the mucosa between the muscular layers. They are classified according to their etiology, as traction and pulsion diverticula.

[FIG. 99.—Traction diverticulum of the esophagus rendered visible in the roentgenogram by a swallowed opaque mixture. Case of H. W. Dachtler, Am. Journ. Roentgenology.]

Traction diverticulum of the esophagus (Fig. 99) is a rare condition, usually occurring in the thorax, and as a rule constituting a one-sided enlargement of the gullet rather than a true pouch formation. It is supposed to be formed by the pulling during cough, respiration, and swallowing, on localized adhesions of the esophagus to periesophageal structures, such as inflammatory peribronchial glands.

Diagnosis is often incidental to examination of the gastrointestinal tract for other conditions, because traction diverticula usually cause no symptoms. Unless a very large esophagoscope be used, a traction diverticulum may easily be overlooked in the mucosal folds. Careful lateral search, however, will reveal the dilatation, and the localized periesophageal fixation may be demonstrated. The subdiverticular esophagus is readily followed, its lumen opening during inspiration unless very close to the diaphragm, which is very rare. Perhaps most cases will be discovered by the roentgenologist. It has been said that traction diverticula are more readily demonstrated in the roentgenologic examination, if the patient be placed with pelvis elevated.

Pulsion diverticulum of the esophagus is an acquired hernia of the mucosa between the circular and oblique fibers of the inferior constrictor muscle of the pharynx. A congenital anatomic basic factor in etiology probably exists. The pouching develops in the middle part of the posterior wall, between the orbicular and oblique fibers of the cricopharyngeus muscle, at which point there is a gap, leaving the mucosa supported only by a not very resistant fascia (Fig. 100). When small, the sac is in the midline, but with increase in size, it presents either to the right or the left side, commonly the latter. The sac may be very small, or it may be sufficiently large to hold a pint or more, and to cause the neck to bulge when filled. When large, the pouch extends into the mediastinum. It will be seen that anatomically the pulsion diverticulum has its origin in the pharynx; the symptoms, however, are referable to the esophagus and the subdiverticular esophagus is stenosed by compression of the pouch; therefore, it is properly classified as an esophageal disease.

[FIG. 100.—Schema illustrative of the etiology of pressure diverticula. O, oblique fibers of the cricopharyngeus attached to the thyroid cartilage, T. The fundiform fibers, F, encircle the mouth of the esophagus. Between the two sets of fibers is a gap in the support of the esophageal wall, through which the wall herniates owing to the pressure of food propelled by the oblique fibers, O, advance of the bolus being resisted by spasmodic contraction of the orbicular fibers, F.]

Etiology.—Pressure diverticula occur after middle life, and more often in men than in women. The hasty swallowing of unmasticated food, too large a bolus, defective or artificial teeth, flaccidity of tissues, and spasm of the cricopharyngeus muscle, are etiologic factors. Cicatricial stenosis below the level of the inferior constrictor is a contributory cause in some cases.

Prognosis.—After the pouch is formed, it steadily increases in size, since the swallowed food first fills and distends the sac before the overflow passes down the esophagus. When a pendulous sac becomes filled with food, it presses on the subdiverticular esophagus, and produces compression stenosis; so that there exists a "vicious circle." The enlargement of the sac produces increasing stenosis with consequent further distension of the pouch. This explains the clinically observed fact, that unless treated, pulsion diverticula increase progressively in size, and consequently in distressing symptoms. The sac becomes so large in some cases as to contribute to the occurrence of cerebral apoplexy by interference with venous return. Practically all cases can be cured by radical operation. The operative mortality varies with the age, state of nutrition, and general health of the patient. In general it may be said to have a mortality of at least 10 per cent, largely due to the fact that most cases are poor surgical subjects. Recurrences after radical operation are due to a persistence of the original causes, i.e., bolting of food; stenosis, spasmodic or organic, of the esophageal lumen; and weakness in the support of the esophageal wall, which, unsupported, has little strength of its own.

Symptoms.—Dysphagia, regurgitation, a gurgling sound and subjective bubbling sensation on swallowing, sour odor to the breath, and cough, are the chief symptoms. With larger pouches, emaciation, pressure sensation in the neck and upper mediastinum, and the presence of a mass in the neck when the sac is filled, are present. Tracheal compression by the filled pouch may produce dyspnea. The sac may be emptied by pressure on the neck, this means of relief being often discovered by the patient. The sac sometimes spontaneously empties itself by contraction of its enveloping muscular layer, and one of the most annoying symptoms is the paroxysm of coughing, waking the patient, when during the relaxation of sleep the sac empties itself into the pharynx and some of its contents are aspirated into the larynx. There are no pathognomonic symptoms. Those recited are common to other forms of esophageal stenosis, and are urgent indications for diagnostic esophagoscopy.

Diagnosis.—Roentgenray study with barium mixtures, is the first step in the diagnosis (Fig. 101). This is to be followed by diagnostic esophagoscopy. Malignant, spasmodic, cicatricial, and compression stenosis are to be excluded by esophagoscopic appearances. Aneurysm is to be eliminated by the usual means. The Boyce sign is almost invariably present, and is diagnostic. It is elicited by telling the patient to swallow, which action imprisons air in the sac. The imprisoned air is forced out by finger-pressure on the neck, over the sac. The exit of the air bubble produces a gurgling sound audible at the open mouth of the patient.

Esophagoscopic Appearances in Pulsion Diverticulum.—The esophagoscope will without difficulty enter the mouth of the sac which is really the whole bottom of the pharynx, and will be arrested by the blind end of the pouch, the depth of which may be from 4 to 10 cm. In some cases the bottom of the pouch is in the mediastinum. The walls are often pasty, and may be eroded, or ulcerated, and they may show vessels or cicatrices. On withdrawing the tube and searching the anterior wall, the subdiverticular slit-like opening of the esophagus will be found, though perhaps not always easily. The esophageal speculum will be found particularly useful in exposing the subdiverticular orifice, and through this a small esophagoscope may be passed into the esophagus, thus completing the diagnosis. Care must be exercised not to perforate the bottom of the diverticular pouch by pressure with the esophagoscope or esophageal speculum. The walls of the sac are surprisingly thin.

[FIG. 101.—Pulsion diverticulum filled with bismuth mixture in a man of fifty years.]

Treatment of Pulsion Diverticulum.—If the pouch is small, the subdiverticular esophageal orifice may be dilated with esophagoscopic bougies, thus overcoming the etiologic factor of spastic or organic stenosis. The redundancy remains, however, though the symptoms may be relieved. Cutting the common wall between the esophagus and the sac by means of scissors passed through the endoscopic tube, has been successfully done by Mosher.

Various methods of external operation have been devised, among which are: (1) Freeing the sac through an external cervical incision and suturing its fundus upward against the pharynx, which has proved successful in some cases. (2) Inversion of the sac into the pharynx and suture of the mouth of the pouch. In a case so treated the pouch was blown out again during a fit of sneezing eight months after operation. (3) Plication of the walls of the sac by catgut sutures, as in the Matas obliterative operation for aneurysm. (4) Freeing and removing the sac, with suture of the esophageal wound. (5) Removal of the sac by a two-stage operation, in which method the initial step is the deliverance of the sac into the cervical wound, where it remains surrounded by gauze packing until adhesions have walled off the mediastinum. The work is completed by cutting off the sac and either suturing the esophageal wound or touching it with the cautery, and allowing it to heal by granulation. External exposure and amputation of the sac has been more frequently done than any other operation. Unless the pouch is large, it is extremely difficult to find after the surgeon has exposed the esophagus, for the reasons that at operation it is empty and that when the adhesions about it are removed the walls of the sac contract. After removal, the sac is disappointingly small as compared with its previous size in the roentgenogram, which shows it distended with opaque material. It has been the chagrin of skilled surgeons to find the diverticulum present functionally and roentgenographically precisely the same as before the performance of the very trying and difficult operation. The time of operation may be shortened at least by one-half by the aid of the esophagoscopist in the Gaub-Jackson operation. Intratracheally insufflated ether is the anesthesia of choice. After the surgeon has exposed the esophagus by dissection, the endoscopist introduces the esophagoscope into the sac, and delivers it into the wound, while the surgeon frees it from adhesions. The esophagoscope is now withdrawn from the pouch and entered into the esophagus proper, below the diverticulum, while the surgeon cuts off the hernial sac and sutures the esophagopharyngeal wound over the esophagoscope. The presence of the esophagoscope prevents too tight suture and possible narrowing of the lumen (Fig. 102).

[FIG. 102.—Schematic representation of esophagoscopic aid in the excision of a diverticulum in the Gaub-Jackson operation. At A the esophagoscope is represented in the bottom of the pouch after the surgeon has cut down to where he can feel the esophagoscope. Then the esophagoscopist causes the pouch to protrude as shown by the dotted line at B. After the surgeon has dissected the sac entirely loose from its surroundings, traction is made upon the sac as shown at H and the esophagoscope is inserted down the lumen of the esophagus as shown at C. The esophagoscope now occupies the lumen which the patient will need for swallowing. It only remains for the surgeon to remove the redundancy, without risk of removing any of the normal wall. The esophagoscope here shown is of the form squarely cut off at the end. The standard form of instrument with slanted end will serve as well.]

After-care.—Feeding may be carried on by the placing of a small nasal feeding tube into the stomach at the time of operation. Gastrostomy for feeding as a preliminary to the esophageal operation has been suggested, and is certainly ideal from the viewpoint of nutrition and esophageal rest. The decision of its performance may perhaps be best made by the patient himself. Should leakage through the neck occur, the fistula should be flushed by the intake of sterile water by mouth. Oral sepsis should, of course, be treated before operation and combated after operation by frequent brushing of the teeth and rinsing of the mouth with Dakin's solution, one part, to ten parts of peppermint water. A postoperative barium roentgenogram should be made in every case as a matter of record and to make certain the proper functioning of the esophagus.



[268] CHAPTER XXXIV—DISEASES OF THE ESOPHAGUS (Continued)

PARALYSIS OF THE ESOPHAGUS

The passage of liquids and solids through the esophagus is a purely muscular act, controlled, after the propulsive usually voluntary start given to the bolus by the inferior constrictor, by a reflex arc having connection with the central nervous system through the vagus nerve. Gravity plays little or no part in the act of deglutition, and alone will not carry food or drink to the stomach. Paralysis of the esophagus may be said to be motor or sensory. It is rarely if ever unassociated with like lesions of contiguous organs.

Motor paralysis of the esophagus is first manifested by inability to swallow. This is associated with the accumulation of secretion in the pyriform sinuses (the author's sign of esophageal stenosis) which overflows into the larynx and incites violent coughing. Motor paralysis may affect the constrictors or the esophageal muscular fibers or both.

Sensory paralysis of the esophagus by breaking the continuity of the reflex arc, may so impair the peristaltic movements as to produce aphagia. The same filling of the pyriform sinuses will be noted, but as the larynx is usually anesthetic also, it may be that no cough is produced when secretions overflow into it.

Etiology.—1. Toxic paralysis as in diphtheria. 2. Functional paralysis as in hysteria. 3. Peripheral paralysis from neuritis. 4. Central paralysis, usually of bulbar origin. Embolism or thrombosis of the posterior cerebral artery is a reported cause in two cases. Lues is always to be excluded as the fundamental factor in the groups 3 and 4. Esophageal paralysis is not uncommon in myasthenia gravis.

Esophagoscopic findings are those of absence of the normal resistance at the cricopharyngeus, flaccidity and lack of sensation of the esophageal walls, and perhaps adherence of particles of food to the folds. The hiatal contraction is usually that normally encountered, for this is accomplished by the diaphragmatic musculature. In paralysis of sensation, the reflexes of coughing, vomiturition and vomiting are obtunded.

Diagnosis.—Hysteria must not be decided upon as the cause of dysphagia, until after esophagoscopy has eliminated paralysis. Dysphagia after recent diphtheria should suggest paralysis of the esophagus. The larynx, lips, tongue, and pharynx also, are usually paralyzed in esophageal paralysis of bulbar origin. The absence of the cricopharyngeal resistance to the esophagoscope passed without anesthesia, general or local, is diagnostic.

Treatment.—The internist and neurologist should govern the basic treatment. Nutrition can be maintained by feeding with the stomach-tube, which meets no resistance to its passage. Should this be contraindicated by ulceration of the esophagus, gastrostomy should be done.

LUES OF THE ESOPHAGUS

Esophageal syphilis is a rather rare affection, and may show itself as a mucous plaque, a gumma, an ulceration, or a cicatrix. Cicatricial stenosis developing late in life without history of the swallowing of escharotics or ulcerative lesions is strongly suggestive of syphilis, though the late manifestation of a congenital stenosis is a possibility.

Esophagoscopic appearances of lues are not always characteristic. As in any ulcerative lesion, the inflammatory changes of mixed infections mask the basic nature. The mucous plaque has the same appearance as one situated on the velum, and gummata resemble those seen in the mucosa elsewhere. There is nothing characteristic in luetic cicatrices.

The diagnosis of luetic lesions of the esophagus, therefore, depends upon the history, presence of luetic lesions elsewhere, the serologic reaction, therapeutic test, examination of tissue, and the demonstration of the treponema pallidum. The therapeutic test by prolonged saturation of the system with mercury is imperative in all suspected cases and no other negative result should be deemed sufficient.

The treatment of luetic esophagitis is systemic, not local. Luetic cicatrices contract strongly, and are very resistant to treatment, so that esophagoscopic bouginage should be begun as early as possible after the healing of a luetic ulceration, in order to prevent stenosis. A silk-woven endoscopic bougie placed in position by ocular guidance, and left in situ for from half to one hour daily, may prevent severe contraction, if used early in the stage of cicatrization. Prolonged treatment is required for the cure of established luetic cicatricial stenosis. If gastrostomy has been done retrograde bouginage (Fig. 35) may be used.

TUBERCULOSIS OF THE ESOPHAGUS

Esophageal tuberculosis is not commonly met, but is probably not infrequently associated with the dysphagia of tuberculous laryngitis. It may rarely occur as a primary infection, but usually the esophagus is involved in an extension from a tuberculous process in the larynx, mediastinal lymphatics, pleura, bronchi, or lungs.

Primary lesions appear as superficial erosions or ulcerations, with a surrounding yellowish granular zone, or the granules may alone be present. The mucosa in tuberculous lesions is usually pallid, the absence of vascularity being marked. Invasion from the periesophageal organs produces more or less localized compression and fixation of the esophagus. The character of open ulceration is modified by the mixed infections. Healed tuberculous lesions, sometimes resulting from the evacuation of tuberculous mediastinal lymph nodes into the esophagus may be encountered. The local fixation and cicatricial contraction may be the site of a traction diverticulum. Tuberculous esophago-bronchial fistulae are occasionally seen.

Diagnosis, to be certain, requires the demonstration of the tubercule bacilli and the characteristic cell accumulation of the tubercle in a specimen of tissue removed from the lesion. Actinomycosis must be excluded, and the possibility of mixed luetic and tuberculous lesions is to be kept in mind. Post-tuberculous cicatrices have no recognizable characteristics.

Treatment.—The maintenance of nutrition to the highest degree, and the institution of a strict antituberculous regime are demanded. Local applications are of no avail. Gastrostomy for feeding should be done if dysphagia be severe, and has the advantage of putting the esophagus at rest. The passage of a stomach-tube for feeding purposes may be done, but it is often painful, and is dangerous in the presence of ulceration. Pain is not marked if the lesion be limited to the esophagus, though if it is present orthoform, anesthesin, or apothesin, in powder form, swallowed dry, may prove helpful.

VARIX AND ANGIOMA OF THE ESOPHAGUS

These lesions are sometimes the cause of esophageal hemorrhage, the regurgitated blood being bright red, and alkaline in reaction, in contradistinction to the acid "coffee ground" blood of gastric origin. Esophageal varices may coexist with the common dilatation of the venous system in which the veins of the rectum, scrotum, and legs are most conspicuously affected. Cirrhosis and cancer of the liver may, by interference with the portal circulation, produce dilatation of the veins in the lower third of the esophagus. Angioma of the esophagus is amenable to radium treatment.

ACTINOMYCOSIS OF THE ESOPHAGUS

Esophageal actinomycosis has been autoptically discovered. Its diagnosis, and differentiation from tuberculosis, would probably rest upon the microscopic study of tissue removed esophagoscopically, though as yet no such case has been reported.

ANGIONEUROTIC EDEMA

Angioneurotic edema involving the esophagus, may produce intermittent and transient dysphagia. The lesions are rarely limited to the esophagus alone; they may occur in any portion of the gastrointestinal, genitourinary, or respiratory tracts, and concomitant cutaneous manifestations usually render the diagnosis clear. The treatment is general.

DEVIATION OF THE ESOPHAGUS

Deviation of the esophagus may be marked in the presence of a deformed vertebral column, though dysphagia is a very uncommon symptom. The lack of esophageal symptoms in deviation of spinal production is probably explained by the longitudinal shortening of the spine which accompanies the deflection. Compression stenosis of the esophagus is commonly associated with deviations produced by a thoracic mass.

[PLATE IV

A, Gastroscopic view of a gastrojejunostomy opening drawn patulous by the tube mouth. (Gastrojejunostomy done by Dr. George L. Hays.) B, Carcinoma of the lesser curvature. (Patient afterward surgically explored and diagnosis verified by Dr. John J. Buchanan.) C, Healed perforated ulcer. (Patient referred by Dr. John W. Boyce.)

Drawn from a case of postdiphtheric subglottic stenosis cured by the author's method of direct galvanocauterization of the hypertrophies. A, Immediately after removal of the intubation tube; hypertrophies like turbinals are seen projecting into the subglottic lumen. B, Five minutes later; the masses have now closed the lumen almost completely. The patient became so cyanotic that a bronchoscope was at once introduced to prevent asphyxia. C, The left mass has been cauterized by a vertical application of the incandescent knife. D, Completely and permanently cured after repeated cauterizations. Direct view; recumbent patient.

PHOTOPROCESS REPRODUCTIONS OF THE AUTHOR'S OIL-COLOR DRAWINGS FROM LIFE]



[273] CHAPTER XXXV—GASTROSCOPY

The stomach of any individual having a normal esophagus and normal spine can be explored with an open-tube gastroscope. The adult size esophagoscope being 53 cm. long will reach the stomach of the average individual. Longer gastroscopes are used, when necessary, to explore a ptosed stomach. Various lens-system gastroscopes have been devised, which afford an excellent view of the walls of the air-inflated stomach. The optical system, however, interferes with the insertion of instruments, so that the open-tube gastroscope is required for the removal of gastric foreign bodies, the palpation of, or sponging secretions from, gastric lesions. The open-tube gastroscope may be closed with a window plug (Fig. 6) having a rubber diaphragm with a central perforation for forceps, when it is desired to inflate the stomach.

Technic.—Relaxation by general anesthesia permits lateral displacement of the dome of the diaphragm along with the esophagus, and thus makes possible a wider range of motion of the distal end of the gastroscope. All of the recent gastroscopies in the Bronchoscopic Clinic, however, have been performed without anesthesia. The method of introduction of the gastroscope through the esophagus is precisely the same as the introduction of the esophagoscope (q.v.). It should be emphasized that with the lens-system gastroscopes, the tube should be introduced into the stomach under direct ocular guidance, without a mandrin, and the optical apparatus should be inserted through the tube only after the stomach has been entered. Blind insertion of a rigid metallic tube into the esophagus is an extremely dangerous procedure.

The descriptions and illustrations of the stomach in anatomical works must be disregarded as cadaveric. In the living body, the empty stomach is usually found, on endoscopic inspection, to be a collapsed tube of such shape as to fit whatever space is available at the particular moment, with folds and rugae running in all directions, the impression given as to form being strikingly like searching among a mass of earth worms or boiled spaghetti. The color is pink, under proper illumination, if no food is present. Poor illumination may make the color appear deep crimson. If food is present, or has just been regurgitated, the color is bright red. To appreciate the appearance of gastritis, the eye must have been educated to the endoscopic appearances under a degree of illumination always the same. The left two-thirds of the stomach is most easily examined. The stomach wall can be pushed by the tube into almost any position, and with the aid of gentle external abdominal manipulation to draw over the pylorus it is possible to examine directly almost all of the gastric walls except the pyloric antrum, which is reachable in relatively few cases. A lateral motion of from 10 to 17 cm. can be imparted to the gastroscope, provided the diaphragmatic musculature is relaxed by deep anesthesia. The stomach is explored by progressive traverse. That is, after exploring down to the greater curvature, the tube-mouth is moved laterally about 2 centimeters, and the withdrawing travel explores a new field. Then a lateral movement affords a fresh field during the next insertion. This is repeated until the entire explorable area has been covered. Ballooning the stomach with air or oxygen is sometimes helpful, but the distension fixes the stomach, lessens the mobility of the arch of the diaphragm, and thus lessens the lateral range of gastroscopic vision. Furthermore, ballooning pushes the gastric walls far away from the reach of the tube-mouth. A window plug (Fig. 6) is inserted into the ocular end of the gastroscope for the ballooning procedure.

[275] Like many other valuable diagnostic means, gastroscopy is very valuable in its positive findings. Negative results are entitled to little weight except as to the explorable area.

The gastroscopist working in conjunction with the abdominal surgeon should be able to render him invaluable assistance in his work on the stomach. The surgeon with his gloved hand in the abdomen, by manipulating suspected areas of the stomach in front of the tube-mouth can receive immediately a report of its interior appearance, whether cancerous, ulcerated, hemorrhagic, etc.

Lens-system ballooning gastroscopy may possibly afford additional information after all possible data from open-tube gastroscopy has been obtained. Care must be exercised not to exert an injurious degree of air-pressure. The distended portion of the stomach assumes a funnel-like form ending at the apex in a depression with radiating folds, that leads the observer to think he is looking at the pylorus. The foreshortening produced by the lens system also contributes to this illusion. The best lens-system gastroscope is that of Henry Janeway, which combines the open-tube and the lens system.

Gastroscopy for Foreign Bodies.—The great majority of foreign bodies that reach the stomach unassisted are passed per rectum, provided the natural protective means are not impaired by the administration of cathartics, changes in diet, etcetera. This, however, does not mean that esophageal foreign bodies should be pushed into the stomach by blind methods, or by esophagoscopy, because a swallowed object lodged in the esophagus can always be returned through the mouth. Foreign bodies in the stomach and intestines should be fluoroscopically watched each second day. If an object is seen to lodge five days in one location in the intestines, it should be removed by laparotomy, since it will almost certainly perforate. Certain objects reaching the stomach may be judged too large to pass the pylorus and intestinal angles. These should be removed by gastroscopy when such decision is made. It is to be remembered that gastric foreign bodies may be regurgitated and may lodge in the esophagus, whence they are easily removed by esophagoscopy. The double-planed fluoroscope of Manges is helpful in the removal of gastric foreign bodies, but there is great danger of injury to the stomach walls, and even the peritoneum, unless forceps are used with the utmost caution.



[277] CHAPTER XXXVI—ACUTE STENOSIS OF THE LARYNX

Etiology.—Causes of a relatively sudden narrowing of the lumen of the larynx and subjacent trachea are included in the following list. Two or more may be combined. 1. Foreign body. 2. Accumulation of secretions or exudate in the lumen. 3. Distension of the tissues by air, inflammatory products, serum, pus, etc. 4. Displacement of relatively normal tissues, as in abductor paralysis, congenital laryngeal stridor, etcetera. 5. Neoplasms. 6. Granulomata.

Edema of the larynx may be at the glottic level, or in the supraglottic or subglottic regions. The loose cellular tissue is most frequently concerned in the process rather than the mucosal layer alone. In children the subglottic area is very vascular, and swelling quickly results from trauma or inflammation, so that acute stenosis of the larynx in children commonly has its point of narrowing below the cords. Dyspnea, and croupy, barking, cough with no change in the tone or pitch of the speaking voice are characteristic signs of subglottic stenosis. Edema may accompany inflammation of either the superficial or deep structures of the larynx. The laryngeal lesion may be primary, or may complicate general diseases; among the latter, typhoid fever deserves especial mention.

Acute laryngeal stenosis complicating typhoid fever is frequently overlooked and often fatal, for the asthenic patient makes no fight for air, and hoarseness, if present, is very slight. The laryngeal lesion may be due to cordal immobility from either paralysis or inflammatory arytenoid fixation, in the absence of edema. Perichondritis and chondritis of the laryngeal cartilages often follow typhoid ulceration of the larynx, chronic stenosis resulting.

Laryngeal stenosis in the newborn may be due to various anomalies of the larynx or trachea, or to traumatism of these structures during delivery. The normal glottis in the newborn is relatively narrow, so that even slight encroachment on its lumen produces a serious degree of dyspnea. The characteristic signs are inspiratory indrawing of the supraclavicular fossae, the suprasternal notch, the epigastrium, and the lower sternum and ribs. Cyanosis is seen at first, later giving place to pallid asphyxia when cardiac failure occurs. Little air is heard to enter the lungs, during respiratory efforts and the infant, becoming exhausted by the great muscular exertion, soon ceases to breathe. Paralytic stenosis of the larynx sometimes follows difficult forceps deliveries during which stretching or compression of the recurrent nerves occur.

Acute laryngeal stenosis in infants, from laryngeal perichondritis, may be a delayed result of traumatism to the laryngeal cartilages during delivery. The symptoms usually develop within four weeks after birth. Lues and tuberculosis are possible factors to be eliminated by the usual methods.

Surgical Treatment of Acute Laryngeal Stenosis.—Multiple puncture of acute inflammatory edema, while readily performed with the laryngeal knife used through the direct laryngoscope, is an uncertain measure of relief. Tracheotomy, if done low in the neck, will completely relieve the dyspnea. By its therapeutic effect of rest, it favors the rapid subsidence of the inflammation in the larynx and is the treatment to be preferred. Intubation is treacherous and unreliable except in diphtheritic cases; but in the diphtheritic cases it is ideal, if constant skilled watching can be had.



[279] CHAPTER XXXVII—TRACHEOTOMY

Indications.—Tracheotomy is indicated in dyspnea of laryngotracheal origin. The cardinal signs of this form of dyspnea are: 1. Indrawing at the suprasternal notch. 2. Indrawing around the clavicles. 3. Indrawing of the intercostal spaces. 4. Restlessness. 5. Choking and waking as soon as the aid of the voluntary respiratory muscles ceases in falling to sleep. 6. Cyanosis is a dangerously late symptom.

As a therapeutic measure in diseases of the larynx its place has been thoroughly established. Marked improvement of the laryngeal lesions has been observed to follow tracheotomy in advanced laryngeal tuberculosis, and in cancer of the larynx. It has proven, in some cases, a useful adjunct in the treatment of luetic laryngitis, though it cannot be regarded as indicated, in the absence of dyspnea. Perichondritis and other inflammations are benefited by tracheotomy. A marked therapeutic effect on multiple laryngotracheal papillomata in children has been noted by the author in hundreds of cases.

Tracheotomy for foreign body is no longer indicated either for the removal of the intruder, or for the insertion of the bronchoscope. Tracheotomy may be urgently indicated for foreign body dyspnea, but not for foreign body removal.

Subcutaneous rupture of the trachea from external trauma may produce dyspnea and generalized emphysema, both of which will be relieved by tracheotomy.

[280] Acromegalic stenosis of the larynx is a rare but urgent indication for tracheotomy.

Contraindications.—There are no contraindications to tracheotomy for dyspnea.

The instruments required for an orderly tracheotomy are: Headlight Scalpels 2 Retractors Trousseau dilator 6 Hemostats Scissors (dissecting) Tracheal cannulae (six sizes) Curved needles Needle holder Hypodermic syringe for local anesthesia No. 1 plain catgut ligatures Linen tape Gauze sponges

These are sterilized and kept in a sterile copper box ready for instant use. Beside the patient's bed following the tracheotomy the following sterile materials are placed: Sterile gloves 1 Hemostat Sterile new gauze Trousseau dilator Scissors Duplicate tracheotomy tube Silver probe Basin of Bichloride of mercury solution, 1 : 10,000

Tracheotomy is one of the oldest operations known to surgery, yet strange to say, it is probably more often improperly performed today, and more often followed by needless mortality, than any other operation. The two chief preventable sequelae are death from improper routine surgical care and wrongly fitted tube, and stenosis from too high an operation. The classical descriptions of crico-thyroidotomy and high and low tracheotomy have been handed down to generations of medical students without revision. Every medical graduate has been taught that there are two kinds of tracheotomy, high and low, the low operation being very difficult, the high operation very easy. When he is suddenly called upon to do an emergency tracheotomy, this erroneous teaching is about all that remains in the dim recesses of his memory; consequently he makes sure of doing the operation high enough, and goes in through the larynx, usually dividing the cricoid cartilage, the only complete ring in the trachea. As originally made the distinction between high and low as applied to tracheotomy referred to operations above and below the isthmus of the thyroid gland, in a day when primitive surgery attached too much importance to operations upon the thyroid gland. The isthmus is entitled to absolutely no consideration whatever in deciding the location at which to incise so vital a structure as the trachea. Students are taught different short skin incisions for these two operations, and it is no wonder that they, as did their predecessors, find tracheotomy a difficult, bloody, and often futile operation. The trachea is searched for at the bottom of a short, deep wound filled with blood, the source of which is difficult to find and impossible to control.